Abstract

INTRODUCTION: Illicit use of anabolic androgenic steroids (AAS) has been growing among athletes and bodybuilders for cosmetic and performance purposes. We report a case of one of the possible hepatic complications of AAS, acute cholestatic syndrome (ACS), in a male with anabolic steroid abuse. CASE DESCRIPTION/METHODS: 27-year-old Polish man with no past medical history presented with jaundice, itching of the body, dark-colored urine, clay-colored stools for 5 weeks. No abdominal pain was reported. Patient reported taking for 4 months 4 types of AAS (testosterone, oxandrolone, methasterone and trenbolone) for body building, which he stopped taking 6 weeks prior to initial presentation due to fatigue. Vitals were normal, and on exam he appeared to be a muscular, jaundiced male with scratch marks on his skin. Abdominal exam revealed a non-tender, non-distended abdomen, with difficulty palpating the liver edge due to the muscularity. Laboratory tests were significant for total bilirubin of 34.8 mg/dL with direct of 23.5 mg/dL, AST 55 U/L, ALT 70 U/L, ALP 212 U/L, GGT 57 U/L, INR 1, creatinine 1.1 mg/dL. Liver ultrasound showed hepatomegaly with no biliary dilation and patent hepatic and portal veins. A liver biopsy was obtained showing portal neutrophil predominant inflammation with occasional eosinophils, mild portal fibrosis and cholestasis, suggestive of drug-induced hepatotoxicity. Liver function tests normalized after 4 months of cessation of AAS use, with resolution of his jaundice and pruritis. DISCUSSION: Body builders usually prefer polydrug use of AAS to maximize the desired effects and hypothetically reduce side effects at the same time. But contrary to their belief, the concomitant use of different illicit AAS may be a factor in their toxicity, making difficult to link an adverse effect with a specific substance. Acute cholesta tic syndrome, has been associated with use of the 17α – alkylated anabolic steroids ( i.e. oxandrolone, methasterone), thought related to an increase of reactive oxygen. This leads to prolonged direct toxic effects and intrahepatic cholestasis, though the pathophysiology remains unclear. ACS usually occurs 1-4 months after steroid initiation presenting with nausea, fatigue, pruritis; later, jaundice, dark urine, with significantly elevated total bilirubin and ALP but mild aminotransferase elevation can be seen. Management consists of stopping anabolic steroid use, supportive care and symptomatic treatment of pruritis.

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